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Reply to Drug Insight: antioxidant therapy in inherited ataxias

Arising from: Pandolfo M (2008) Drug Insight: antioxidant therapy in inherited ataxias. Nat Clin Pract Neurol 4: 86–96 doi:10.1038/ncpneuro0704

Author's response: Pandolfo M (2008) Author response to “Reply to Drug Insight: antioxidant therapy in inherited ataxias”. Nat Clin Pract Neurol 4: E2 doi:10.1038/ncpneuro0834

We read with great interest and curiosity the recent Review entitled Drug Insight: antioxidant therapy in inherited ataxias.1 We acknowledge that the review criteria included the search terms “vitamin E” and “oxidative stress”, and on the basis of these criteria, are inclined to overlook Professor Pandolfo's assertion that vitamin E is an antioxidant (page 90). We are, however, very concerned that the Review ignores scientific literature that questions the antioxidant role of vitamin E.2,3,4

More importantly, recent studies suggest that chronic vitamin E deficiency in a mouse model of ataxia with vitamin E deficiency (AVED) decreases superoxide production from mitochondria and decreases oxidative stress in the brain.5 The lungs6 and heart7 of the AVED mouse also show a lack of oxidative stress. To the best of our knowledge, there is not a single study in AVED humans that has assayed markers of oxidative stress in the affected tissue. Vitamin E deficiency should, therefore, not be equated with increased oxidative stress.

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Correspondence to Kishorchandra Gohil.

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Gohil, K., Azzi, A. Reply to Drug Insight: antioxidant therapy in inherited ataxias. Nat Rev Neurol 4, E1 (2008). https://doi.org/10.1038/ncpneuro0833

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